How long for lowered prolactin levels (from dostinex) come back to normal levels?
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hhajdo
Community Veteran
Clin Endocrinol (Oxf) 1988 Nov;29(5):467-76 Related Articles, Links
Long-lasting lowering of serum growth hormone and prolactin levels by single and repetitive cabergoline administration in dopamine-responsive acromegalic patients.
"Cabergoline induced a marked fall in serum PRL level, starting within 3 h and continuing for 7 days after administering 0.3 mg, and for 14 days after 0.6 mg."
----------------------------------------------------
Prolactin-lowering effect of acute and once weekly repetitive oral administration of cabergoline at two dose levels in hyperprolactinemic patients.
Mattei AM, Ferrari C, Baroldi P, Cavioni V, Paracchi A, Galparoli C, Romano C, Spellecchia D, Gerevini G, Crosignani PG.
.."One group (n = 26) received 0.3 mg, and the other (n = 25) received 0.6 mg. Both cabergoline doses induced a significant fall in serum PRL levels, which lasted, on the average, from 3 h to 5 days after 0.3 mg and from 3 h to 14 days after 0.6 mg;..."
Long-lasting lowering of serum growth hormone and prolactin levels by single and repetitive cabergoline administration in dopamine-responsive acromegalic patients.
"Cabergoline induced a marked fall in serum PRL level, starting within 3 h and continuing for 7 days after administering 0.3 mg, and for 14 days after 0.6 mg."
----------------------------------------------------
Prolactin-lowering effect of acute and once weekly repetitive oral administration of cabergoline at two dose levels in hyperprolactinemic patients.
Mattei AM, Ferrari C, Baroldi P, Cavioni V, Paracchi A, Galparoli C, Romano C, Spellecchia D, Gerevini G, Crosignani PG.
.."One group (n = 26) received 0.3 mg, and the other (n = 25) received 0.6 mg. Both cabergoline doses induced a significant fall in serum PRL levels, which lasted, on the average, from 3 h to 5 days after 0.3 mg and from 3 h to 14 days after 0.6 mg;..."
I am wrapping up my post cycle of test and deca with the use of dostinex e3d and aromisin ed adn will be getting blood work in a month or so. I was wondering if there would be a large nolva like rebound for the dostinex when stopped. I am going to use it at 1 pill e/w for the rest of my post recovery just to be safe.
DROID
DROID
hhajdo
Community Veteran
droid said:
Some people have slightly elevated PRL post cycle, but that rarely happens.
IMO you shouldn't use cabergoline unless you know that your PRL is elevated.
It's a very strong drug which can cause your PRL too drop to much which can negatively affect HPTA recovery.
There shouldn't be a rebound when you stop it.
If you still want to use it one pill per week should be enough.
E3D would definitely decrease your PRL too much.
Last edited:
Fonz
Elite Mentor,
hhajdo said:
I've found that 0.625-1.25mg Bromocriptine ED post-cycle helps with HPTA recovery as most people see a slight elevation in prolactin levels during and post-cycle. The aforementioned Bromocriptine dosage should just bring your prolactin levels back to normal. Also, it does give you a slight anorectic effect w/o the dreaded nausea/grogginess 2.5mg+ ED Bromo normally gives you.
Fonz
hhajdo
Community Veteran
Welcome to the board bro..
I don't think that most people will have elevated PRL post/during the cycle.
If you keep your estrogen in normal range during the cycle your PRL should stay normal, or even drop since androgens in general don't elevate & sometimes actually lower PRL.
One doc on another board said that he had a few patiens whose PRL was elevated post cycle, & did not have successful normalization of LH and testosterone levels post cycle unless prolactin was also normalized ... so it can happen...
Very few studies have addressed this (I've only seen two)...
The PRL of the guy in this study, for example, was in low normal range post cycle...
Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.
Fertil Steril. 2003 Jan;79(1):203-5
...A 30-year-old patient presented with severe depression and loss of libido and energy. He admitted to the use of steroids for bodybuilding purposes for several months. He had obtained nandrolone decanoate, deca Durabolin, primobolan depot, and Winstrol from a foreign country without a prescription...
.. Just before clomiphene citrate administration, laboratory examination revealed a total T of 71 ng/dL (reference range, 260–1000 ng/dL), free T of 29 pg/dL (reference range, 34–194 pg/dL), bioavailable T of 61 ng/dL (reference range, 84–402 ng/dL), LH of 3.7 miu/mL (reference range, 1.5–9.3 miu/mL), FSH of 2.4 miu/mL (reverence range 1.4–18.1 miu/mL), prolactin of 5 ng/mL (reference range, 2–18 ng/mL), and TSH of 1.36 miu/mL (reference range, 0.40–5.50 miu/mL)....
I don't think that most people will have elevated PRL post/during the cycle.
If you keep your estrogen in normal range during the cycle your PRL should stay normal, or even drop since androgens in general don't elevate & sometimes actually lower PRL.
One doc on another board said that he had a few patiens whose PRL was elevated post cycle, & did not have successful normalization of LH and testosterone levels post cycle unless prolactin was also normalized ... so it can happen...
Very few studies have addressed this (I've only seen two)...
The PRL of the guy in this study, for example, was in low normal range post cycle...
Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.
Fertil Steril. 2003 Jan;79(1):203-5
...A 30-year-old patient presented with severe depression and loss of libido and energy. He admitted to the use of steroids for bodybuilding purposes for several months. He had obtained nandrolone decanoate, deca Durabolin, primobolan depot, and Winstrol from a foreign country without a prescription...
.. Just before clomiphene citrate administration, laboratory examination revealed a total T of 71 ng/dL (reference range, 260–1000 ng/dL), free T of 29 pg/dL (reference range, 34–194 pg/dL), bioavailable T of 61 ng/dL (reference range, 84–402 ng/dL), LH of 3.7 miu/mL (reference range, 1.5–9.3 miu/mL), FSH of 2.4 miu/mL (reverence range 1.4–18.1 miu/mL), prolactin of 5 ng/mL (reference range, 2–18 ng/mL), and TSH of 1.36 miu/mL (reference range, 0.40–5.50 miu/mL)....
Fonz
Elite Mentor,
SWALE said:
If the cycle consisted of Anabolic Androgenic Steroids (AAS) that were only ER and PRagonists then I'd agree.
But it seems that Anabolic Androgenic Steroids (AAS) that are prolactin agonists(Fina) do cause a post-cycle rise in prolactin.
SPECIALLY trenbolone. I already posted as to why people start lactating while on Tren......and its b/c of the elevated prolactin levels.
This is another reason why Tren is immuno-suppresive. It causes prolactin levels to rise. Prolactin has been directly linked to immuno-supression.....and HPTA suppression.
Using Bromo(Or Cabergoline) while on Fina is not only warranted but I believe crucial in restoring your immune system back to near normal during the cycle, and restoring your HPTA after the cycle.
Fonz
hhajdo
Community Veteran
There is no evidence that tren affects PRL levels.
Both hyperprolactinemia and hypoprolactinemia are immunosuppressive, so by taking bromo & similar drugs without supervision you might screw up your immune system & HPTA at the same time.
Neuroimmunomodulation 1997 Jul-Aug;4(4):171-80 Related Articles, Links
Action of pituitary and lymphocyte prolactin.
Matera L.
Department of Internal Medicine, University of Turin, Italy. matera@molinette.unito.it
In vivo and in vitro data combined show that prolactin (PRL) can mimic or interact with known lymphocyte cytokines and that these, in turn, can regulate PRL synthesis at the site of immune response. In contrast, pituitary PRL is under the control of both immune system products (non-cognitive stimuli) and signals to the CNS (cognitive stimuli). The role of PRL as a cytokine and as an endocrine hormone is discussed. In particular, assignment of PRL to the T helper 1 phenotype is proposed, based on its ability to enhance NK cell function, activate the interferon-regulated factor (IRF-1) transcription factor and to interact with or generate IL-2 and IFN gamma. Since hyperprolactinemia and hypoprolactinemia are both immunosuppressive, physiological levels of circulating PRL must be necessary to maintain normal immunocompetence. Moderate increases in PRL during immune stimulation of the hypothalamic-pituitary axis may counteract glucocorticoid inhibition, whereas inappropriate prolongation of PRL synthesis could lead to autoimmune diseases...
Stimulation of in vivo antibody production and concanavalin-A-induced mouse spleen cell mitogenesis by prolactin.
Spangelo BL, Hall NR, Ross PC, Goldstein AL
Department of Biochemistry, George Washington University Medical School, Washington, D.C. 20037.
Regulation of the immune system by neuroendocrine hormones is receiving increased attention. Prolactin, a hormone normally associated with lactation, has been shown recently to reconstitute immunosuppressed hypophysectomized rats. The present studies demonstrate that prolactin administration to normal mice results in a biphasic stimulation of antibody production to sheep red blood cells. While 100 and 200 micrograms bovine prolactin/animal stimulated antibody production, 400 micrograms had no effect. Potentiation of lectin-induced T-cell mitogenesis by prolactin was also biphasic. As the concentration of prolactin increased the incorporation of [3H]thymidine into the cells first increased and then decreased. Decreasing serum prolactin levels with the dopaminergic agonist bromocriptine resulted in a reduction of antibody titers to sheep erythrocytes and a modulation of thymic weight. These data show that prolactin can stimulate the immune system in a biphasic manner and that a reduction in the basal levels of this hormone results in an attenuated immune response.
Both hyperprolactinemia and hypoprolactinemia are immunosuppressive, so by taking bromo & similar drugs without supervision you might screw up your immune system & HPTA at the same time.
Neuroimmunomodulation 1997 Jul-Aug;4(4):171-80 Related Articles, Links
Action of pituitary and lymphocyte prolactin.
Matera L.
Department of Internal Medicine, University of Turin, Italy. matera@molinette.unito.it
In vivo and in vitro data combined show that prolactin (PRL) can mimic or interact with known lymphocyte cytokines and that these, in turn, can regulate PRL synthesis at the site of immune response. In contrast, pituitary PRL is under the control of both immune system products (non-cognitive stimuli) and signals to the CNS (cognitive stimuli). The role of PRL as a cytokine and as an endocrine hormone is discussed. In particular, assignment of PRL to the T helper 1 phenotype is proposed, based on its ability to enhance NK cell function, activate the interferon-regulated factor (IRF-1) transcription factor and to interact with or generate IL-2 and IFN gamma. Since hyperprolactinemia and hypoprolactinemia are both immunosuppressive, physiological levels of circulating PRL must be necessary to maintain normal immunocompetence. Moderate increases in PRL during immune stimulation of the hypothalamic-pituitary axis may counteract glucocorticoid inhibition, whereas inappropriate prolongation of PRL synthesis could lead to autoimmune diseases...
Stimulation of in vivo antibody production and concanavalin-A-induced mouse spleen cell mitogenesis by prolactin.
Spangelo BL, Hall NR, Ross PC, Goldstein AL
Department of Biochemistry, George Washington University Medical School, Washington, D.C. 20037.
Regulation of the immune system by neuroendocrine hormones is receiving increased attention. Prolactin, a hormone normally associated with lactation, has been shown recently to reconstitute immunosuppressed hypophysectomized rats. The present studies demonstrate that prolactin administration to normal mice results in a biphasic stimulation of antibody production to sheep red blood cells. While 100 and 200 micrograms bovine prolactin/animal stimulated antibody production, 400 micrograms had no effect. Potentiation of lectin-induced T-cell mitogenesis by prolactin was also biphasic. As the concentration of prolactin increased the incorporation of [3H]thymidine into the cells first increased and then decreased. Decreasing serum prolactin levels with the dopaminergic agonist bromocriptine resulted in a reduction of antibody titers to sheep erythrocytes and a modulation of thymic weight. These data show that prolactin can stimulate the immune system in a biphasic manner and that a reduction in the basal levels of this hormone results in an attenuated immune response.
Fonz
Elite Mentor,
hhajdo said:
#1 Yes, there is. A lot of people get a white milky discharge from their nipples during Tren cycles. This can only be caused by elevated prolactin.
#2. Agreed. Prolactin levels have to be within the normal range.
Problem with 99% of the people who use Anabolic Androgenic Steroids (AAS) is that they don't get blood-tests.......
My PRL levels certainly went up on Tren. Not by a lot....but they did.
More so than any other Anabolic Androgenic Steroids (AAS) in my case.
Fonz
If Tren is indeed a PRL agonist, then it does not elevate PRL while the agonist is being administered. In fact, it would decrease production of same, depending upon its affinity amongst the variety of PRL receptors found in the body.
Last edited:
hhajdo
Community Veteran
I really don't think that tren is a PRL agonist.
The impact of other possible factors on PRL secretion shouldn't be underestimated...
Stress, meds (some antipsychotic drugs & antihypertensive drugs can significantly increase it, etc..)
Too much paranoia based on a lamb study, IMO.
Even some animal studies indicate that "TBA implantation of the pregnant ewe produced dystocia and less milk production "
Effect of prenatal trenbolone acetate treatment on lamb performance and carcass characteristics.
DeHaan KC, Berger LL, Kesler DJ, McKeith FK, Thomas DL.
I agree with Fonz that blood-tests are very important.
Taking bromo/cabergoline without monitoring your PRL levels is a bad idea...
The impact of other possible factors on PRL secretion shouldn't be underestimated...
Stress, meds (some antipsychotic drugs & antihypertensive drugs can significantly increase it, etc..)
Too much paranoia based on a lamb study, IMO.
Even some animal studies indicate that "TBA implantation of the pregnant ewe produced dystocia and less milk production "
Effect of prenatal trenbolone acetate treatment on lamb performance and carcass characteristics.
DeHaan KC, Berger LL, Kesler DJ, McKeith FK, Thomas DL.
I agree with Fonz that blood-tests are very important.
Taking bromo/cabergoline without monitoring your PRL levels is a bad idea...
Fonz
Elite Mentor,
hhajdo said:
Not directly......no. Indirectly.....yes.
The increased PRL levels are a feed-back mechanism that stems from trenbolones anti-glucocorticoid activity.
The higher the Fina dosage...the more you reduce endo cortisone...the higher your PRL levels.
At least in my case. And I have done dosages ranging from 37.5mg ED to 300mg ED.
Obviously, peoples reactions to Anabolic Androgenic Steroids (AAS) are different. But I do believe there is a perfect Tren dosage for everybody. i.e. A small but insignificant elevation in PRL levels, yet good anti-glucocorticoid activity for you to reap the anti-catabolic benefits of tren.
Fonz
Fonz
hhajdo
Community Veteran
Although AS affect cortisol synthesis in vitro, their impact in vivo is not that significant.
The anti-glucocorticoid activity is caused by glucocorticoid receptor antagonism.
All AS in general antagonize the glucocorticoid receptor...
Testosterone, dihydrotestosterone, trenbolone acetate, and zeranol alter the synthesis of cortisol in bovine adrenocortical cells.
Department of Animal Science, University of Nebraska, Lincoln 68583-0908.
...The objective of this study was to examine the effect of anabolic steroids (testosterone, T; dihydrotestosterone, D; trenbolone acetate, B; and zeranol, Z) on cortisol synthesis by cultured bovine adrenocortical cells...
.."The suppression of cortisol synthesis did not differ between B and T or between B and D...
In vivo:
Use of trenbolone acetate and estradiol in intact and castrate male cattle: effects on growth, serum hormones, and carcass characteristics.
Hunt DW, Henricks DM, Skelley GC, Grimes LW.
Clemson University, SC 29634.
The effects of anabolic implant on growth, carcass characteristics, and serum hormones were examined in 30 young bulls and steers fed a growing diet then a finishing diet. In a 2 X 3 factorial arrangement, steers and bulls received an implant of trenbolone acetate (TBA), TBA and estradiol-17 beta (E2), or no implant. Blood samples were taken serially (every 20 min for 6 h) at intervals during the growing and finishing phases. Percentage of DM, fat, protein, and ash and Warner-Bratzler shear test were measured and taste panel evaluations of the 9-10-11 rib section were obtained. Treatment with TBA and E2 increased weight gain in steers but not in bulls. There were no differences in feed efficiency, serum growth hormone (GH), and cortisol concentrations between bulls and steers or between treated groups and controls in bulls or steers
--------------------------------------
The effect of manipulating growth in sheep by diet or anabolic agents on plasma cortisol and muscle glucocorticoid receptors.
.." 3. Trenbolone acetate treatment reduced the binding capacity of sheep skeletal muscle for cortisol within 2 d of implantation..."
--------------------------------------
Also
J Steroid Biochem 1988 Jun;29(6):575-81 Related Articles, Links
Evidence for sex-dependent anabolic response to androgenic steroids mediated by muscle glucocorticoid receptors in the rat.
..The results suggest that anabolic steroids can act via muscle glucocorticoid receptors, thereby antagonizing the catabolic activity of endogenous glucocorticoids...
-------------------------------------
And
Am J Physiol 1975 Nov;229(5):1381-6 Related Articles, Links
Interaction of anabolic steroids with glucocorticoid receptor sites in rat muscle cytosol.
Mayer M, Rosen F.
While glucocorticoid hormones act catabolically on skeletal muscle through their binding to glucocorticoid-specific receptors in the cytosol, androgens exert anabolic responses but no androgen-specific binding proteins could be detected in this responsive tissue. However, various nonradioactive androgens were effective in displacing labeled dexamethasone or cortisol from their respective cytoplasmic receptors in muscle, both in vitro and in vivo. The inhibition of glucocorticoid binding by androgens is competitive, and could be observed following a single or repeated administration of the androgens to adrenalectomized-castrated animals. The synthetic androgen fluoxymesterone and the hormone testosterone displayed Ki values of 7.5 X 10(-6) M and 1 X 10(-5) M, respectively, for the inhibition of [3H]dexamethasone binding in muscle cytosol. On the basis of competition experiments it is postulated that interaction of androgens with glucocorticoid receptors prevents the binding of glucocorticoids and might be responsible in part for the anabolic effects of pharmacologic doses of androgens in muscle.
If testosterone treatment causes PRL increase, for example, that increase doesn't have much to do with its glucocorticoid receptor antagonism, it's caused by elevated estrogen and can be prevented by use of SERMs or aromatase inhibitors...
The anti-glucocorticoid activity is caused by glucocorticoid receptor antagonism.
All AS in general antagonize the glucocorticoid receptor...
Testosterone, dihydrotestosterone, trenbolone acetate, and zeranol alter the synthesis of cortisol in bovine adrenocortical cells.
Department of Animal Science, University of Nebraska, Lincoln 68583-0908.
...The objective of this study was to examine the effect of anabolic steroids (testosterone, T; dihydrotestosterone, D; trenbolone acetate, B; and zeranol, Z) on cortisol synthesis by cultured bovine adrenocortical cells...
.."The suppression of cortisol synthesis did not differ between B and T or between B and D...
In vivo:
Use of trenbolone acetate and estradiol in intact and castrate male cattle: effects on growth, serum hormones, and carcass characteristics.
Hunt DW, Henricks DM, Skelley GC, Grimes LW.
Clemson University, SC 29634.
The effects of anabolic implant on growth, carcass characteristics, and serum hormones were examined in 30 young bulls and steers fed a growing diet then a finishing diet. In a 2 X 3 factorial arrangement, steers and bulls received an implant of trenbolone acetate (TBA), TBA and estradiol-17 beta (E2), or no implant. Blood samples were taken serially (every 20 min for 6 h) at intervals during the growing and finishing phases. Percentage of DM, fat, protein, and ash and Warner-Bratzler shear test were measured and taste panel evaluations of the 9-10-11 rib section were obtained. Treatment with TBA and E2 increased weight gain in steers but not in bulls. There were no differences in feed efficiency, serum growth hormone (GH), and cortisol concentrations between bulls and steers or between treated groups and controls in bulls or steers
--------------------------------------
The effect of manipulating growth in sheep by diet or anabolic agents on plasma cortisol and muscle glucocorticoid receptors.
.." 3. Trenbolone acetate treatment reduced the binding capacity of sheep skeletal muscle for cortisol within 2 d of implantation..."
--------------------------------------
Also
J Steroid Biochem 1988 Jun;29(6):575-81 Related Articles, Links
Evidence for sex-dependent anabolic response to androgenic steroids mediated by muscle glucocorticoid receptors in the rat.
..The results suggest that anabolic steroids can act via muscle glucocorticoid receptors, thereby antagonizing the catabolic activity of endogenous glucocorticoids...
-------------------------------------
And
Am J Physiol 1975 Nov;229(5):1381-6 Related Articles, Links
Interaction of anabolic steroids with glucocorticoid receptor sites in rat muscle cytosol.
Mayer M, Rosen F.
While glucocorticoid hormones act catabolically on skeletal muscle through their binding to glucocorticoid-specific receptors in the cytosol, androgens exert anabolic responses but no androgen-specific binding proteins could be detected in this responsive tissue. However, various nonradioactive androgens were effective in displacing labeled dexamethasone or cortisol from their respective cytoplasmic receptors in muscle, both in vitro and in vivo. The inhibition of glucocorticoid binding by androgens is competitive, and could be observed following a single or repeated administration of the androgens to adrenalectomized-castrated animals. The synthetic androgen fluoxymesterone and the hormone testosterone displayed Ki values of 7.5 X 10(-6) M and 1 X 10(-5) M, respectively, for the inhibition of [3H]dexamethasone binding in muscle cytosol. On the basis of competition experiments it is postulated that interaction of androgens with glucocorticoid receptors prevents the binding of glucocorticoids and might be responsible in part for the anabolic effects of pharmacologic doses of androgens in muscle.
If testosterone treatment causes PRL increase, for example, that increase doesn't have much to do with its glucocorticoid receptor antagonism, it's caused by elevated estrogen and can be prevented by use of SERMs or aromatase inhibitors...
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